Study: When a frightening memory is connected with smell, this trigger can be used to reactivate the memory during sleep.

Sleep can reactivate fearful memories and alleviate them, according to a new
mice model research. This finding, the researchers say, could lead to the
development of more effective treatments for post-traumatic stress disorder
(PTSD). It was presented recently at Neuroscience 2012, the annual meeting of
the Society for Neuroscience and the most extensive source of neuroscience and
brain health news.

The study finds that when a frightening memory is
connected with smell, this trigger – the smell – can be used to reactivate the
memory during sleep without actually interrupting the sleep. The researchers –
Dr. Asya Rolls of the Rappaport Faculty of Medicine at the Technion- Israel
Institute of Technology in Haifa and Megha Makam of the research groups headed
by Profs. H. Craig Heller and Luis de Lecea of Stanford University – found that
if the reactivation is repeated, the frightening memory is strengthened; but if
the re-creation is accompanied by a treatment that blocks the creation of
proteins in the basolateral amygdala, the area of the brain associated with
fear, the frightening memory is weakened.

PTSD is characterized by
intense, highly emotional memories that are awakened by specific social and
environmental triggers.

In extinction therapy, the patient repeatedly
re-creates the memory in nonthreatening surroundings, such as a clinic; however,
the treatment is sometimes identified with the clinic to the extent that it
ceases to be effective, and the patient experiences the traumatic trigger
elsewhere, such as while out on the street.

“Sleep is not linked to a
specific location, and thus changes that occur in traumatic memories during
sleep could weaken the fear response regardless of where the memory awakens,”
Heller explains.

“This fact could provide a significant solution to the
limitations of existing PTSD treatments.”

In their experiments,
researchers created conditioning that paired certain smells with an electrical
shock in mice while they were awake. This “control smell” was also released in
the mice’s cages while they were asleep in the presence of a protein synthesis
inhibitor. The activation of the conditioning smell during sleep resulted in a
substantial reduction in the fear response in later tests, while the mice were
awake. Most important, the decrease in the fear response was general and was not
connected to a specific location.

“This is where the significant
potential of the treatment of traumas during sleep actually lies. While we
sleep, our brain works differently, some of our protective systems are not
activated, which, in principle, allows us to access associations which might not
be accessible to treatment while we are awake,” says Rolls.

“Moreover,
many treatments terminate prematurely because the patient finds it difficult to
deal with the repeated mention of the traumatic memories. Therefore, treatment
during sleep could be an easier alternative to dealing with such memories. Of
course, there is still quite a distance between these preliminary experiments
and actually treating people, but it is a start.”